<?xml version="1.0" encoding="UTF-8"?>
<rss xmlns:creativeCommons="http://backend.userland.com/creativeCommonsRssModule" xmlns:atom="http://www.w3.org/2005/Atom" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" version="2.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:media="http://search.yahoo.com/mrss/">
  <channel>
    <title>Nature Precedings - Tag feed for physiology</title>
    <link>http://precedings.nature.com/tags/physiology</link>
    <description>Recently posted documents tagged with 'physiology'</description>
    <dc:publisher>Nature Publishing Group</dc:publisher>
    <dc:language>en</dc:language>
    <prism:publicationName>Nature Precedings</prism:publicationName>
    <image>
      <title>Nature Precedings</title>
      <url>http://precedings.nature.com/images/header_logo.gif</url>
      <link>http://precedings.nature.com</link>
    </image>
    <atom:link type="application/rss+xml" rel="self" href="http://precedings.nature.com/tags/physiology/feed"/>
    <item>
      <title>The beauty of the mammalian vascular system</title>
      <link>http://precedings.nature.com/documents/2976/version/1</link>
      <description>Beauty is a characteristic of objects that provides a perceptual experience of pleasure. In nature, aesthetic appreciation thereof has given rise to the mathematical search for good series (e.g. the Fibonacci series) and proportions (e.g. the Golden proportion) as important elements of beauty. In 1928 the mathematician George David Birkhoff introduced a formula for aesthetic measurement of an object. Birkhoff equation defines the aesthetic value as the amount of order divided by the complexity of the product. These two features can be measured easily in poetry, music, painting, architecture, etc. In the fine arts, it is the artist who manipulates both these features, but how does nature manage order and complexity in living organisms or their parts? Here we show how Birkhoff equation, applied to the mammalian vascular system of eight representative animals, results in new insights into the organization of the animal vascular system. We found that order and complexity are highly correlated in the mammalian vascular system (R2=0.9511). Accordingly, in nature both features are not independently managed in the manner of artists. We found significant differences among the Birkhoff aesthetic values in the mammalian arterial system, whereas no such differences exist in the venous system. We anticipate our approach to be useful in the study of morphogenesis and evolution of tree-like structures, employing the Birkhoff aesthetic value as a simple tool for conducting such studies.</description>
      <guid>http://precedings.nature.com/documents/2976/version/1</guid>
      <pubDate>Wed, 25 Mar 2009 20:02:54 UTC</pubDate>
      <dc:title>The beauty of the mammalian vascular system</dc:title>
      <dc:identifier>hdl:10101/npre.2009.2976.1</dc:identifier>
      <dc:date>2009-03-25</dc:date>
      <dc:creator>Rafael Lahoz-Beltra</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-03-25T20:02:54Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Developmental Biology</prism:section>
      <media:thumbnail url="http://precedings.nature.com/documents/2976/version/1/files/npre20092976-1.pdf.thumb.png"/>
      <creativeCommons:license>http://creativecommons.org/licenses/by/3.0/</creativeCommons:license>
    </item>
    <item>
      <title>Chronic cocaine enhances release of neuroprotective amino acid taurine: a microdialysis study</title>
      <link>http://precedings.nature.com/documents/2319/version/1</link>
      <description>Cocaine inhibits high-affinity neurotransmitter uptake at the presynaptic nerve terminals to increase synaptic levels of dopamine, norepinephrine and serotonin1. This increase of synaptic dopamine may cause neurotoxicity2,3. At least two different mechanisms have been proposed for the development of dopamine-related neurotoxicity: 1) dopamine produces a free radical that may induce cell toxicity2,3 and 2) dopamine reduces glutamate transport at its presynaptic sites to increase synaptic levels of this amino acid4 and augments glutamate transmission by activating dopamine D1 receptors in different areas of the brain5-7. Increase in glutamatergic transmission mediated by the activation on N-methyl dextro-aspartate (NMDA) receptors has been shown to cause excitotoxicity and neuro-degeneration8. Others and we have reported protection against different psychotropic drug-induced neurotoxicity that may be achieved by prior or simultaneous administration of various pharmacological agents. For example, repeated treatment of rats with haloperidol induced neuronal damage that is ameliorated by prior administration of either GM1 ganglioside9 or the endogenous amino acid, taurine10. Similarly, chronic gestational cocaine exposure causes neurotoxicity that could be prevented by co-administration of clozapine11. To our knowledge, there is no information if chronic cocaine would enhance release of endogenous protective agents that may oppose the over activation of glutamatergic system. Here we show that repeated cocaine treatment increased synaptic levels of the neuroprotective amino acid taurine that opposes the excessive excitatory actions of the glutamatergic system in the rat brain. Thus, mammalian brain has an auto-protective mechanism to counter excitotoxicity and taurine or its synthetic derivative may be useful in the management and treatment of cocaine addiction and its neurotoxic effect.</description>
      <guid>http://precedings.nature.com/documents/2319/version/1</guid>
      <pubDate>Wed, 24 Sep 2008 10:21:20 UTC</pubDate>
      <dc:title>Chronic cocaine enhances release of neuroprotective amino acid taurine: a microdialysis study</dc:title>
      <dc:identifier>hdl:10101/npre.2008.2319.1</dc:identifier>
      <dc:date>2008-09-24</dc:date>
      <dc:creator>Mervan Agovic</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2008-09-24T10:21:20Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Neuroscience</prism:section>
      <prism:section>Pharmacology</prism:section>
      <media:thumbnail url="http://precedings.nature.com/documents/2319/version/1/files/npre20082319-1.pdf.thumb.png"/>
      <creativeCommons:license>http://creativecommons.org/licenses/by/3.0/</creativeCommons:license>
    </item>
    <item>
      <title>Physiological Mechanisms Underlying Motion-Induced Blindness</title>
      <link>http://precedings.nature.com/documents/1506/version/1</link>
      <description>Visual disappearance illusions &amp;#8211; such as motion-induced blindness (MIB) &amp;#8211; are commonly used to study the neural underpinnings of visual perception. In such illusions a salient visual target becomes perceptually invisible. Previous studies are inconsistent regarding the role of primary visual cortex (V1) in these illusions. Here we provide physiological and psychophysical evidence supporting a role for V1 in generating MIB.</description>
      <guid>http://precedings.nature.com/documents/1506/version/1</guid>
      <pubDate>Wed, 09 Jan 2008 22:11:41 UTC</pubDate>
      <dc:title>Physiological Mechanisms Underlying Motion-Induced Blindness</dc:title>
      <dc:identifier>hdl:10101/npre.2008.1506.1</dc:identifier>
      <dc:date>2008-01-09</dc:date>
      <dc:creator>Camilo Libedinsky</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2008-01-09T22:11:41Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Neuroscience</prism:section>
      <media:thumbnail url="http://precedings.nature.com/documents/1506/version/1/files/npre20081506-1.pdf.thumb.png"/>
      <creativeCommons:license>http://creativecommons.org/licenses/by/3.0/</creativeCommons:license>
    </item>
  </channel>
</rss>
